Successfully superior mesenteric artery stenting in operated type A aortic dissection complicated with delayed mesenteric malperfusion.

Here, we describe a case of a 61-year-old male patient with acute type A aortic dissection involving the ascending aorta, aortic arch, descending aorta, and the abdominal aorta down to the iliac bifurcation with evidence of left common iliac artery occlusion. Computed tomography angiography revealed progressive dissection into the superior mesenteric artery and left renal artery with no clinical signs of mesenteric ischemia. Emergent ascending aortic reconstruction of the dissected aorta relieves the leg ischemia. On a postoperative day 9, the evolution was complicated by massive right hemothorax. Although the patient was hemodynamically stable after obtaining hemostasis, the patient developed paralytic ileus with a high elevated lactate level. Visceral malperfusion was not detected by exploratory laparotomy. Emergency abdominal aortic angiography revealed superior mesenteric artery intermittent occlusion, successfully treated by stenting implantation.

Rare tumors of the heart--angiosarcoma, pericardial lipoma, leiomyosarcoma. Three case reports.

Primary tumors of the heart, pericardium and inferior vena cava are extremely rare. Three cases of surgically/biopsy proven angiosarcoma of the right atrium, pericardial lipoma and leiomyosarcoma of inferior vena cava--demonstrated by ultrasound, computed tomography (CT) and magnetic resonance imaging (MRI)--are presented here.

Congenital short QT syndrome. A review.

Sudden cardiac death in individuals with structurally normal hearts accounts for approximately 20% of sudden cardiac death cases. Patients in this subgroup suffer from what has been named "electrical diseases" which are gradually coming into focus as inherited ion channelopathies, diseases of anchoring proteins or of intracellular calcium regulating proteins. From 1993, the Short QT Syndrome (SQTS) came to our attention, as a new inherited "electrical disease" associated with increased risk of sudden cardiac death and atrial fibrillation. Mutations of Ikr, Iks, Ikl channels cause dysfunctional Iks, Ikr, Ikl channels with an increase in the net outward K current leading to shortening of repolarization. This in turn leads to a shorter QT interval on the ECG and shorter atrial and ventricular refractory periods with increased susceptibility to VF and AF. There seems to be an autosomal dominant mode of inheritance. The clinical profile of SQTS consists of: family history of sudden cardiac death, personal history of palpitations, syncope, dizziness, resuscitated SCD, history of AF and documented VF. It is important to emphasize that SQTS is symptomatic from early age (new-born) to old age. Therefore, it is possible that SQTS accounts for some of the sudden infant death syndrome cases and for some cases of AF, especially lone AF. The only efficient treatment for ventricular arrhythmias is ICD, associated with drugs (Quinidine or Propaphenone) for AF prophylaxis and for reducing the number of ventricular arrhythmic events (and ICD discharges).